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Operative Treatment
INDICATIONS
Surgery generally is indicated unless favorable circumstances allow for conservative treatment trial:
Definitive indications: colonic perforation, progressive dilation, abdominal compartment syndrome, beginning
multiorgan dysfunction.
Lack of response or deterioration within 3–5 days of conservative treatment.
OPERATIVE APPROACH
Total abdominal colectomy with end-ileostomy (ie, sparing rectum and pelvic dissection).
Turnbull blowholes: more of historical than practical interest as it leaves the disease burden on the patient.
Outcome
True toxic megacolon still carries high mortality:
Any resection less than total colectomy is associated with poor outcome.
Decision to operate comes too late!
Poor prognostic parameters: secondary organ dysfunction, perforation, peritonitis, coagulopathy, delayed
intervention.
If patient is still hemodynamically stable and not coagulopathic
mortality has dropped from 30% to 1%.
Probability that patient will require colectomy: 50–90% (depending on series).
Follow-Up
Emergency surgery: planning of subsequent surgeries after complete physical/nutritional recovery.
Recovery with conservative management: close monitoring of clinical course, elective surgery?
Cross-Reference
Colitis or proctitis (Ch. 1)
Large bowel obstruction (LBO) (Ch. 1), (Ch. 4)
Megacolon (Ch. 1)
Conventional x-rays (plain film) (Ch. 2)
Computed tomography (CT scan) (Ch. 2)
Ischemic colitis (557.X) (Ch. 4)
Pseudomembranous/Clostridium difficile colitis (008.45) (Ch. 4)
IBD—ulcerative colitis (556.9) (Ch. 4)
Colonic pseudoobstruction (Ogilvie syndrome, 560.89) (Ch. 4)
Total abdominal colectomy with end-ileostomy (open) (Ch. 5)
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Medical management of ulcerative colitis (Ch. 5)
Medications against tumor or inflammation (App. 1)
LARGE BOWEL OBSTRUCTION (LBO, 560.9)
Overview
LBO is a partial or complete mechanical obstruction distal to the ileocecal valve. Complete LBO: no passage of stool and gas.
Partial LBO: abdominal distention, cramping, but still occasional passage of gas or stool.
Numerous causes: neoplasm (intrinsic, extrinsic), benign stricture (chronic diverticulitis, ischemic, radiation, Crohn disease),
adhesions (more often resulting in SBO than LBO), colonic volvulus, intussusception, hernia, endometriosis.
Obliteration of large bowel lumen results in prestenotic stalling of stool. The initial compensatory hypermotility (increased
and tympanitic bowel sounds) weakens and shifts into paralytic ileus (late phase, absence of bowel sounds). Increased
intraluminal pressure results in bowel dilation with subsequent impairment of microcirculation, followed by increased mucosal
permeability and bacterial translocation. Third-spacing of fluids into bowel wall and into the bowel lumen + decreased oral
intake + loss from nausea/vomiting, transudation result in hypotension that perpetuates vicious circle with downward spiral.
Complications: electrolyte and metabolic imbalance, malnutrition, colonic perforation (at site of obstruction, eg, perforating
cancer, or in dilated prestenotic colon, particularly if ileocecal valve competent), colon gangrene, feculent peritonitis, septic
shock.
Epidemiology
Causes: 60–80% malignancies, 10–20% diverticular stricture, 5% colonic volvulus.
Synchronous tumor: in nonobstructing tumors 2–5%; in obstructing cancer 10–25% incidence of synchronous polyps and 5–
10% of synchronous cancers in proximal colon.
Symptoms
Depending on cause: gradual or sudden onset of crampy abdominal pain, distention, constipation followed by lack of passage
of stool and gas, decreased appetite, dehydration, weight loss. Late symptoms: nausea and vomiting (miserere = fecal
vomiting).
Change of stool consistency over course of the colon (right side: soft/liquid, left side: more compact and formed)
earlier
development of clinical symptoms in left-sided colon obstruction.
Differential Diagnosis
SBO, paralytic ileus (eg, pancreatitis).
Constipation (LLQ pain, no fever, no WBC elevation, improvement on Fleet enema, colon full of stool).
Colonic pseudoobstruction (Ogilvie syndrome).
Megacolon (toxic, Hirschsprung, Chagas diseases).
Pathology
Underlying pathology causing the obstruction.
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Evaluation
REQUIRED MINIMAL STANDARD
History: time frame of symptoms, previous similar episodes, change in bowel habits, bleeding per rectum, anemia, last
passage of stool/gas. Previous surgeries (eg, bowel resection, appendectomy, hysterectomy, etc)? Previous colonic
evaluations (flexible sigmoidoscopy, colonoscopy, contrast enema)? Comorbidities (coronary artery disease, COPD, diabetes,
liver/kidney disease, etc).
Clinical examination: vital signs
signs of toxicity, fever? distended/meteoric abdomen, diffuse vs localized tenderness,
guarding and peritoneal signs? Increased and tympanitic bowel sounds? Rectal mass? Inguinal hernia!! Fluid
status/dehydration?
X-rays: supportive but not sufficient to make diagnosis of LBO:
– Upright chest x-ray: free intraperitoneal air?
– Abdominal x-ray: colonic distention; ie, diameter of cecum > 12 cm, transverse colon > 6 cm (1
1
/
2
vertebrae)?
Small bowel distention? Transition point? Evidence of volvulus?
Rigid (or flexible) sigmoidoscopy: always indicated unless perforation.
Lab work: increased WBC? Anemia? Renal failure (prerenal: dehydration; postrenal: obstruction involving urinary system).
Urinalysis: urinary tract infection
sign of fistulizing process?
Limited water-soluble contrast enema (up to obstruction point but not beyond)!:
road map, but risk of perforation if
hyperosmolar contrast trapped proximal to stenosis.
Colonoscopy (with possible stenting): assessment of obstruction site, biopsy, possible stenting (see operative treatment)
full colonic evaluation prior to surgery.
ADDITIONAL TESTS (OPTIONAL)
CT abdomen/pelvis (Figure 4–17A) with dual (oral + IV) or triple (oral + IV + rectal) contrast: site and nature of obstruction,
colonic diameter, pneumatosis coli, extraluminal and free intraperitoneal air? Evidence of tumor spreading (carcinomatosis,
liver metastases), ascites? Assessment of kidneys, NGT, abdominal aorta, visceral arterial blood supply (celiac, SMA, IMA),
portal vein, pleural effusion, etc.
Spiking temperatures: blood cultures.
Fecal occult blood test: only if no macroscopic bleeding per rectum.
Figure 4–17A.
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CT scan of LBO.
Classification
Partial vs complete LBO.
LBO with perforation: at site of obstruction vs distant from obstruction (most commonly in the cecum).
Right-sided LBO vs left-sided LBO.
Nonoperative Treatment
General measures: adequate monitoring, fluid resuscitation, nothing by mouth, NGT placement, IV antibiotics only with
defined target.
Local measures if partial LBO:
Enemas, mild orthograde bowel cleansing.
Volvulus: endoscopic decompression, possible tube placement.
Hernia: attempt to reduction unless incarcerated.
Operative Treatment
INDICATION
Every true LBO is an indication for surgery, unless special circumstances ask for less aggressive approach (eg, end-stage
carcinomatosis):
Complete obstruction emergency.
Partial obstruction semi-urgent, workup possible (eg, full colonic clearance).
Operative Approach
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Disobstruction Without Resection (eg, Incarcerated Hernia)
Need to check colonic viability, resection if in doubt.
Colonic Decompression
Prestenotic colostomy (Figure 4–17B): eg, loop transverse or sigmoid colostomy is simplest (temporary) operation to
allow effective decompression (potentially even in local anesthesia)
stabilization and further investigation of fragile
patients. (Caveat: tube cecostomy is not indicated/sufficient because it does not allow for proper
decompression/elimination of stool).
Stenting of left-sided colonic obstruction: definitive palliation or bridging to (semi-)elective resection 1–2 weeks post
stenting after stabilization, bowel preparation, and colon clearance.
Figure 4–17B.
CT scan of LBO before and after transverse loop colostomy.
Resection
Right-sided obstruction: direct resection with ileocolostomy (regardless of bowel preparation).
Left-sided obstruction:
– Hartmann resection with end-colostomy and blind distal stump.
– Resection with primary anastomosis and proximal diversion.
– (Sub-)total colectomy with ileosigmoidostomy or ileorectostomy.
– Resection with on-table lavage and primary anastomosis.
Outcome
Surgical mortality historically very high (up to 30–40%), more recently 3–14%.
Stenting: successful in ~90%, risk of perforation, migration.
Follow-Up
Confirmation of diagnosis, full colonic evaluation.
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Assess effectiveness of resuscitation (vital signs, urine output).
Planning of subsequent surgeries: after temporary decompression without resection, stoma reversal after discontinuous
resection.
Cross-Reference
Megacolon (Ch. 1)
Small bowel obstruction (SBO) (Ch. 1)
Conventional x-rays (plain film) (Ch. 2)
Computed tomography (CT scan) (Ch. 2)
Colorectal cancer—colon cancer (153.X) (Ch. 4)
Toxic megacolon (556.9) (Ch. 4)
Colonic pseudoobstruction (Ogilvie syndrome, 560.89) (Ch. 4)
Colonic volvulus (560.2) (Ch. 4)
Diverticular disease (diverticulosis, diverticulitis, 562.1X) (Ch. 4)
Sigmoid resection (open, anastomosis vs Hartmann) (Ch. 5)
(Sub-)Total colectomy, ileorectal anastomosis (open) (Ch. 5)
Colonoscopic stent placement (Ch. 5)
On-table lavage for primary anastomosis in LBO (Ch. 5)
Creation of end-ileostomy or -colostomy (Ch. 5)
COLONIC PSEUDOOBSTRUCTION (OGILVIE SYNDROME, 560.89)
Overview
Colonic distention without a mechanical obstruction resulting from acquired diffuse colonic dysmotility disorder, usually
secondary to general illness or surgery. Numerous extrinsic triggering factors in 95% of cases, which typically occur in the
setting of hospitalization or nursing facility: cardiac disease (congestive heart failure, post–cardiopulmonary bypass),
retroperitoneal or mediastinal pathology (hematoma, neoplasia), trauma (eg, spinal fractures), pulmonary disease
(pneumonia, embolus), metabolic disturbances, drug adverse effects (narcotics, anticholinergics, calcium-channel blockers,
antidepressants), extra-abdominal surgeries (eg, orthopedic), prolonged immobility; 5% of cases idiopathic.
Most commonly, pseudoobstruction not associated with any intrinsic colonic pathology, but it can occasionally be a first
manifestation of C difficile or ischemic colitis.
Rupture of cecum is the most frequent complication (La Place law: pressure inversely proportional to diameter). Treatment is
initially conservative including pharmacologic intervention, colonoscopic decompression, rarely surgical.
Epidemiology
Incidence essentially unknown: 0.3–1.5% of major orthopedic procedures. Age generally increasing, average 5th–6th
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decade. Male predominance.
Symptoms
Abdominal distention increasing abdominal discomfort, labored breathing, risk of perforation (mainly in cecum)
peritoneal signs.
Variable symptoms: constipation, diarrhea, nausea/vomiting, tachycardia, progressive weight loss.
Differential Diagnosis
Mechanical LBO: identifiable site of obstruction (transition point).
Toxic megacolon (IBD, C difficile, other colitis): fever, tachycardia, abdominal tenderness, etc.
Nontoxic megacolon (Hirschsprung, Chagas).
Volvulus.
Postoperative ileus.
Pathology
No intrinsic pathology in majority of cases.
Evaluation
REQUIRED MINIMAL STANDARD
History: presence of triggering factors? Past colonic evaluations? Bleeding?
Clinical examination: distended, tympanitic abdomen, presence/absence of bowel sounds, peritoneal signs (
suggestive of
impending perforation) serial abdominal exams.
Abdominal and chest x-ray: colonic distention, free air? If no immediate surgery
serial abdominal x-rays.
At least limited colonic evaluation (water-soluble contrast enema, colonoscopy
also decompression) to rule out distal
obstruction.
ADDITIONAL TESTS (OPTIONAL)
CT scan: if other pathology or complication suspected (eg, abscess, mass, aortic rupture, etc).
C difficile toxin.
Classification
Pseudoobstruction without or with intrinsic colonic pathology.
Compensated vs decompensated colonic contractility.
Nonoperative Treatment
Absence of severe pain or critical colonic distention (> 12 cm cecum, > 6 cm transverse colon):
Optimization of conservative management: treatment of underlying disease, correction of electrolyte imbalances,
bowel rest, IV fluid, nasogastric suction, removal of precipitants (narcotics, anticholinergics, etc).
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Drugs or enemas to stimulate colonic motility.
Alternating body positioning.
Colonic stimulation:
Neostigmine 2 mg IV over 2–4 hours (alternative: IV within 10 minutes).
Side effects (more frequent if shorter administration period): bradycardia, abdominal pain, diaphoresis, salivation,
vomiting.
Precautions: supine position, telemetry monitoring, atropine available as antidote.
Contraindications: mechanical obstruction, perforation, heart rate < 60, bronchospasm.
Colonoscopic decompression (ideally followed by neostigmine):
Diagnostic clarification (rule out obstruction, inflammation, ischemia), rapid decompression (particularly if critical
colonic diameter), potential guidewire-assisted placement of decompression tube.
Operative Treatment
INDICATION
Failed medical and endoscopic management.
Signs of peritonitis.
Perforation: ischemia, serosal splitting, mucosal herniation.
OPERATIVE APPROACH
Not Perforated
Open (vs percutaneous) cecostomy tube placement for venting of the colon (caveat: does not divert stool!).
Creation of loop ileostomy (with decompressive catheter through efferent limb through ileocecal valve into
ascending colon).
Creation of loop colostomy.
Perforated
Total abdominal colectomy with ileostomy.
Hartmann-type procedure.
Outcome
Depending on underlying condition:
Conservative management (including neostigmine): 85–90% success, 20% recurrent distention require repeated
decompression; 3–20% morbidity, 1% (–14%) mortality.
Need for surgical intervention: 5–15% due to intestinal ischemia or perforation higher mortality rate (up to 50%,
comorbidities!).
Follow-Up
Resolution under conservative management: no specific follow-up needed, colonic evaluation per guidelines.
Postsurgical intervention: planning of subsequent surgeries once triggering circumstances eliminated.
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Cross-Reference
Large bowel obstruction (LBO) (Ch. 1), (Ch. 4)
Megacolon (Ch. 1)
Conventional x-rays (plain films) (Ch. 2)
Computed tomography (CT scan) (Ch. 2)
Psuedomembranous/Clostridium difficile colitis (008.45) (Ch. 4)
Toxic megacolon (556.9) (Ch. 4)
"Stomatology"—the science of ostomies (V44.2) (Ch. 4)
Creation of loop ileostomy or colostomy (laparoscopic/open) (Ch. 5)
COLONIC VOLVULUS (560.2)
Overview
Volvulus is a rotation of the colon segment around its pedicle, which may result in obstruction, strangulation, closed loop,
necrosis, and perforation. It is the third most common cause of LBO (3–10%). Subvolvulus with single or recurrent episodes
of incomplete rotation and/or quick spontaneous detorsion: very difficult to verify, may precede manifest volvulus (in up to
50%).
Predisposing factors: anatomic hypermobility due to inadequate retroperitoneal attachments, narrow mesenteric base and
redundant bowel loop, fiber-rich diet (geographic high-incidence zone around equator: "volvulus-belt"). Multiple other
conditions associated with volvulus: age, pregnancy, psychotropic medications, constipation, diarrhea, Parkinson disease,
pregnancy, Chagas disease, peptic ulcer, ischemic colitis, diabetes.
Location: sigmoid volvulus (60–75%) > cecal volvulus (20–35%) > transverse colon (3–5%). Two different mechanisms:
axial rotation (90%, all sites), volvulus en bascule (10%, cecum) = horizontal and upward folding of cecal pole.
Epidemiology
Geographic variation of incidence: 2–5% of all LBO in US, 15–30% (up to 80%) in geographic belt (South America, Africa,
Middle East, India, Pakistan, Eastern Europe). Age in US: 60–70 years, rare in children. Gender: males > females.
Symptoms
Clinical triad:
Acute abdominal pain, often initially crampy in nature.
Abdominal distention.
Cessation of bowel activity.
Late signs: fever, chills, nausea, vomiting, hypotension and shock, peritoneal signs.
Differential Diagnosis
Other causes of LBO:
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Neoplasm (intrinsic, extrinsic).
Stricture (diverticulitis, ischemia, anastomotic, Crohn disease).
Hernia.
Colonic pseudoobstruction.
Fecal impaction.
Other causes of SBO, ileus.
Acute ischemic colitis or mesenteric ischemia.
Pathology
Nonspecific: ischemic changes with vascular congestion, hemorrhage, necrosis.
Evaluation
REQUIRED MINIMAL STANDARD
History: underlying bowel function, time of onset, preceding history of subvolvulus?
Clinical examination: assessment of general hemodynamic condition and fluid status, fever, abdominal distention,
presence/absence of peritoneal signs, bowel sounds hyperperistaltic (early), absent (late). Digital rectal exam: empty rectal
vault.
Imaging:
Abdominal x-ray: diagnostic in 70–90% when dilated colon with "bent inner tube" or "coffee-bean sign" with axis
from LLQ to RUQ (sigmoid volvulus) or RLQ to LUQ (cecal volvulus).
Contrast studies (typically not necessary): "bird's beak" or "ace of spades."
Endoscopy (rigid or flexible): "whirl sign"—spiraling narrow segment
therapeutic attempt to overcome obstruction by
untwisting (particularly for sigmoid volvulus).
ADDITIONAL TESTS (OPTIONAL)
CT: only if diagnosis in doubt (eg, suspected ischemia): "whirl sign," evidence of necrosis (eg, pneumatosis)?
Classification
Based on location: sigmoid vs cecal vs transverse colon.
Based on mechanism: torsion (classical form), cecal volvulus en bascule.
Based on severity: nongangrenous, gangrenous.
Nonoperative Treatment
Sigmoid Volvulus
Rigid proctosigmoidoscopy (or flexible sigmoidoscopy) with rectal tube insertion (eg, chest drain).
Contrast enema.
Colonoscopy.